β-Lactamase producing Gram negative organisms have been an increasing concern in oncology-related infections.

β-Lactamase is commonly produced via 2 mechanisms which constitute the most clinically relevant mechanisms of resistance in gram negative bacilli:

a) Transfer of genetic material encoding for resistance via a plasmid, such as in extended spectrum β-Lactamase producing organisms (ESBL). ESBL are mostly found in E. coli and Klebsiella pneumoniae. In studies looking at the prevalence of ESBL in Klebsiella pneumoniae bloodstream infection in children’s oncology unit, prevalence of ESBL producers represents up to 50% of clinical isolates 38. Major predisposing factors are recent exposure to a 3rd generation cephalosporin containing regimen and prolonged hospital stays.

b) Through the induction of a chromosomally encoded β-Lactamase such as a class C cephalosporinase, also known as AmpC.

AmpC producing Enterobacteriaciae are remembered through the memomentic SPACE:

Serretia spp.

Pseudomonas aeruginosa

Acinetobacter spp.

Citrobacter spp.

Enterobacter spp.

These organisms all have an inducible cephalosporinase and can develop resistance while the patient is on large spectrum antibiotics. There is variability between antibiotics regarding their potential to induce this AmpC enzyme, as well as their lability to its production. Cephalosporin of the 1st generation, ceftazidime and Carbapenems are good inducers, but only carbapenems are not labile to the enzyme produced. The incidence of these various resistant organisms is variable from institution to institution and knowledge of local microbiological data is key in making decisions about appropriate empiric antimicrobial therapy protocols.